Pathophysiology Exam 3

Front 1

Most sensitive area for triggering cough reflex

Back 1

Carina

Front 2

Difference in two bronchi

Back 2

Right primary bronchus is wider, shorter, and more vertical.
Objects usually end up in the right bronchus b/c its an easier pathway.

Front 3

Bronchi and blood vessels enter the lungs where?

Back 3

Hilus

Front 4

Tissues of the bronchioles

Back 4

Smooth muscle
No cartilage
The bronchioles supply the alveoli

Bronchi do contain rings of cartilage.

Front 5

Alveoli

Back 5

The business area of the lungs.
Small thin air sacs surrounded by a hair net of capillaries.
Most of the walls of the alveoli are made of simple squamous epithelium, called type 1 alveolar cells, Gas exchange takes place through these cells.

Front 6

Type II alveolar cells

Back 6

Produce surfactant (lipoprotein) to decrease the surface tension of water in the lungs.

Front 7

Dust cells

Back 7

Alveolar macrophages - phagocytize foreign particles and microbes.

Front 8

Pulmonary ventilation

Back 8

Takes place by decreasing the pressure inside the thoracic cavity, and allowing atm pressure to force air into lungs.
Thoracic cavity is expanded primarily by the the contraction and lowering of the diaphragm, but is aided by expansion of the chest by contraction of the external intercostal muscles.

Front 9

Expiration

Back 9

Normally a passive process due to the relaxing of the inspiratory muscles and the elastic recoil of the lungs.

Front 10

Hypoperfusion

Back 10

Inadequate blood flow to the lungs.

Front 11

Hypoventilation

Back 11

Inadequate air flow to the alveoli.

Front 12

Major causes of nosocomial infections

Back 12

Factors that reduce airflow also compromise particle clearance and predispose to infection.
Restricted lung movement and ventilation may arise due to positioning, constricting bandages, CNS depression, and coma.
There is a high rate of pneumonia in hospital patients b/c of impaired ventilation and clearance.

Front 13

Signs and symptoms of pulmonary disease

Back 13

Dyspnea - subjective sensation of uncomfortable breathing, or feeling SOB. Can range from mild discomfort after exertion to extreme difficulty breathing at rest.
Dyspnea is usually caused by diffuse and extensive rather than focal pulmonary disease.

Front 14

What can cause dyspnea?

Back 14

Dyspnea can be due to airway obstruction so a greater force is needed to provide adequate ventilation.
Constriction or fluid accumulation in the airways can cause a wheezing sound due to air being forced through these airways.
Can be caused by decreased compliance of lung tissue.

Front 15

Signs of dyspnea

Back 15

Flaring nostrils
Use of accessory muscles in breathing.
Retraction, or pulling back, of the intercostal spaces.

Front 16

Cough

Back 16

The attempt to clear the lower respiratory passages by abrupt and forceful expulsion of air.
This is most common when fluid accumulates in the lower airways.

Front 17

What can cause a cough?

Back 17

Inflammation of lung tissue.
Increased secretion in response to mucosal irritation - can be caused by inhalation of irritants, or a intrinsic source of mucosal disruption such as tumor invasion of the bronchial wall.
Excessive blood hydrostatic pressure in pulmonary capillaries - pulmonary edema where excess fluid passes into the airways.

Front 18

hemoptysis

Back 18

Production of bloody sputum.
Usually involves only a small amount of blood loss.
This is not threatening, but can indicate a serious pulmonary disease such as tuberculosis, lung abscess, cancer, or pulmonary infarction.
If sputum is purulent, an infection of lungs or airway is indicated.

Front 19

Chronic cough

Back 19

A cough that persists for more than 3 weeks.
In nonsmokers, almost always due to postnasal drainage syndrome, asthma, or gastroesophageal reflux disease.
In smokers, chronic bronchitis is the most common cause, although lung cancer should be considered.

Front 20

Cyanosis

Back 20

When blood contains a large amount of unoxygenated hemoglobin, it has a dark red-blue color which gives skin a characteristic bluish appearance.
Most cases arise as a result of peripheral vasoconstriction resulting in reduced blood flow, which allows hemoglobin to give up more of its oxygen to tissues - this is referred to as peripheral cyanosis.
This is best seen in the nail beds.
Can be due to a cold environment, anxiety, etc.

Front 21

Central cyanosis

Back 21

Can be due to abnormalities of the respiratory membrane, mismatch b/t air flow and blood flow.
Expressed as a ratio of change in ventilation (V) to perfusion (Q), or V/Q ratio.
Pulmonary thromboembolus can cause reduced blood flow and airway obstruction can result in reduced ventilation.
In persons w/ dark skin this can be seen in the whites of the eyes and mucous membranes.

Front 22

Peripheral cyanosis

Back 22

Most cases of peripheral cyanosis arise as a result of peripheral vasoconstriction - results in reduced blood flow, which allows hemoglobin to give up more its oxygen to tissues.
Best seen in the nail beds.

Front 23

When is cyanosis evident, or observable?

Back 23

In adults, it is not evident until severe hypoxemia is present.
Clinically observable when reduced hemoglobin levels reach 5 g/dl.
Severe anemia and CO poisoning give inadequate oxygenation of tissues w/o cyanosis.
Individuals w/ polycythemia may have cyanosis when oxygenation is adequate.
LACK OF CYANOSIS DOES NOT MEAN OXYGENATION IS NORMAL!

Front 24

Where does pain originate?

Back 24

Originates in the pleurae, airways, or chest wall.
Inflammation of the parietal pleura causes a sharp or stabbing pain when pleura stretches during inspiration - usually localized to an area of the chest wall where a pleural friction rub can be heard.
Common w/ pulmonary infarction due to embolism.

Front 25

Clubbing

Back 25

The selective bulbous enlargement of the end of a digit (finger or toe).
Usually painless.
Commonly assoc'd w/ diseases that cause decreased oxygenation such as lung cancer, cystic fibrosis, lung abscess, or congenital heart disease.

Front 26

Respiratory failure

Back 26

The inability of the lungs to adequately oxygenate the blood and to clear it of carbon dioxide.
Can be acute such as w/ ARDS or pulmonary embolism, direct injury to the lungs, airways, or chest wall, or indirect due to injury of another body system such as the brain or spinal cord.

Front 27

Chronic respiratory failure

Back 27

Due to progressive hypoventilation from airway obstruction or restrictive disease.

Front 28

Why is respiratory failure always serious? What are some signs and symptoms?

Back 28

Nervous tissue is highly oxygen-dependent, so see CNS signs and symptoms such as memory loss, visual impairment, drowsiness, and HA due to increased intracranial pressure due to cerebral vasodilation.
Dysnpea is always present, but it may be difficult to detect a change in a chronic patient.

Front 29

Hypoxic Respiratory Failure

Back 29

Seen when pO2 falls to or below 60mmHg.
Typically seen in chronic bronchitis and emphysema, in lung consolidation due to bacterial infection, or in lung collapse, pulmonary htn, pulmonary embolism, and ARDS.
Initially, produces HA and nervous agitation, soon followed by a decline in mental activity and confusion.
With a progressive lowering of pO2, more widespread tissue damage and loss of consciousness can be expected.
Brain stem hypoxia and renal hypoxia.

Front 30

Brain stem hypoxia

Back 30

In the event of brain stem hypoxia, CNS output to the heart and systemic arterioles can produce circulatory shock.

Front 31

Renal hypoxia

Back 31

Renal hypoxia can cause a loss of homeostatic balance and accumulation of wastes to complicate the problem.

Front 32

Hypoxic-Hypercapnic respiratory failure

Back 32

When arterial pCO2 (normally 40mmHg), exceeds 45mmHg, a condition called hypercapnia.
Most often, obstructive conditions produce this form of respiratory failure, as can hypoventilation from CNS problems, thoracic cage, or neuromuscular abnormalities.

Front 33

How does the body attempt to compensate for hypercapnia? What are some of the effects of this condition?

Back 33

Attempts to compensate include increased heart rate and vasodilation, which produces warm, moist ski.
CNS effects produce muscular tremors, drowsiness and coma.
Hypercapnia also produces acidosis.

Front 34

Acute respiratory distress syndrome (ARDS)

Back 34

Rapid and severe onset of respiratory failure characterized by acute lung inflammation and diffuse injury to the respiratory membrane w/ noncardiogenic edema.
Mortality in persons <60 is 40%.
Those over 65 and immunocompromised still have mortality over 60%.
Most survivors have almost normal lung function 1 year after acute illness.

Front 35

Pathophysiology of ARDS

Back 35

All disorders causing ARDS acutely injure the respiratory membrane and produce severe pulmonary edema, shunting, and hypoxemia.
Damage can occur directly via aspiration of acidic gastric contents or inhalation of toxic gases.
Damage can occur indirectly from chemical mediators from systemic disorders.

Front 36

What is the results of ARDS?

Back 36

Results is massive inflammatory response by the lungs.
Initial injury damages the pulmonary capillary epithelium causing platelet aggregation and intravascular thrombus formation.
Platelets release substances that attract and activate neutrophils.
Damage also activates the complement cascade which also activates neutrophils and the inflammatory response.
Type II alveolar cells are damaged, and surfactant production is decreased - alveoli fill w/ fluid or collapse.
Lungs become less compliant and ventilation decreases.

Front 37

What is shunting?

Back 37

Blow flow is normal, but gas exchanged is decreased. V/Q ratio increases: the same effect as if blood were shunting or bypassing the lungs.

Front 38

Why are neutrophils central to the development of ARDS?

Back 38

Neutrophils release inflammatory mediators such as proteolytic enzymes, toxic oxygen products, prostaglandins and leukotrienes, and platelet activating factors.
These damage the respiratory membrane and increase capillary permeability allowing fluids, proteins, and blood cells to leak into alveoli causing pulmonary edema and hemorrhage reducing pulmonary ventilation and compliance.
Neutrophils and macrophages also release mediators that cause pulmonary vasoconstriction which can results in pulmonary htn.

Front 39

Time span of ARDS

Back 39

After 24-48 hours hyaline membranes form.
After a/b 7 days, fibrosis progressively obliterates the alveoli, respiratory bronchioles and interstitial.
Result is acute respiratory failure.

Front 40

How can ARDS lead to multiple organ dysfunction syndrome (MODS)?

Back 40

Chemical mediators often cause widespread inflammation, endothelial damage and increased capillary permeability throughout the body.
This lead to systemic inflammatory response syndrome, which leads to MODS.
Death may not be caused by ARDS alone, but by MODS.

Front 41

Clinical manifestations of ARDS

Back 41

Symptoms develop progressively and include hyperventilation -> respiratory alkalosis -> dyspnea and hypoxemia - > metabolic acidosis -> respiratory acidosis -> further hypoxemia -> hypotension -> decreased cardiac output -> and ultimately death.

Front 42

Evaluation and treatment of ARDS

Back 42

Diagnosis is based on physical examination, blood gases, and imaging.
Treatment is based on early detection, supportive therapy, and prevention of complications, especially infection.
Mechanical ventilation is often required.
Some studies underway for treatment include prophylactic immunotherapy, Ab's against endotoxins, inhibition of inflammatory mediators, inhalation of NO to reduce pulmonary htn, and surfactant replacement.

Front 43

Postoperative respiratory failure

Back 43

Same pathophysiology as ARDS, but usually not as severe.
Smokers are at risk, esp. if they have a pre-existing lung disease.
Also ppl w/ chronic renal failure, chronic hepatic disease, or infection.
Thoracic and abdominal surgeries carry greatest risk.
Individuals usually have a period of hypotension during surgery, and many have sepsis.

Front 44

Prevention of postoperative respiratory failure

Back 44

Frequent turning
Deep breathing, or spirometry.
Early ambulation to prevent atelectasis and accumulation of secretions.
Humidification of the air to loosen secretions.
Supplemental oxygen and antibiotics as appropriate.
Respiratory failure may require mechanical ventilation for a long time.

Front 45

Obstructive pulmonary disease.

Back 45

Characterized by airway obstruction that is worse w/ expiration. More force is required to expire a given volume of air, or emptying of lungs is slowed, or both.
Most common obstructive diseases are asthma, chronic bronchitis, and emphysema.
Many ppl have chronic bronchitis and emphysema, and together these are often calle chronic obstructive pulmonary disease (COPD).
Main symptom of obstructive pulmonary disease is dyspnea, and the unifying sign is wheezing.
Individuals have increased work of breathing, V/Q mismatching, and a decreased forced expiratory volume.

Front 46

Most common obstructive diseases

Back 46

Asthma, chronic bronchitis, and emphysema.
Chronic bronchitis and emphysema together are allied chronic obstructive pulmonary disease, or COPD.

Front 47

Asthma

Back 47

More intermittent and acute than COPD, even though it can be chronic.
Factor that sets it apart from COPD is its REVERSIBILITY.
Occurs at all ages w/ a/b half developing during childhood.
Runs in families, so genetics may play a role.
Major pathological feature is inflammation resulting in hyper responsiveness of the airways.

Front 48

Major events in an acute asthma attack

Back 48

Bronchiolar constriction, mucus hypersecretion, and inflammatory swelling.
Exposure to allergens or irritants causes mast cells to release granules and trigger the release of many inflammatory mediators such as histamine, interleukins, immunoglobulins, prostaglandins, and NO.
See vasodilation and increased capillary permeability.
Chemotactic factors attract neutrophils, eosinophils, and lymphocytes to the area causing bronchial infiltration.
Production of thick, tenacious mucus.

Front 49

Clinical manifestations of asthma

Back 49

During remission, the individual is asymptomatic and pulmonary function tests are normal.
Dyspnea.
Often a severe cough.
Wheezing exhalation.
Attacks usually of one to two hours duration, but may be severe and continue for days or even weeks.

Front 50

Status asthmaticus

Back 50

If bronchospasms in asthma are not reversed by usual measures, the individual is considered to have severe bronchospasm or status asthmatics.
If this continues it can be life threatening.

Front 51

Management and treatment of asthma

Back 51

Avoid triggers such as allergens and irritants.
Acute attacks are treated w/ corticosteroids and inhaled beta-agonists.
Inhaled bronchodilators,
Immunotherapy such as allergy shots.
Chronic management includes regular use of inhaled anti-inflammatory meds such as corticosteroids, chromolyn sodium, or leukotriene inhibitors.
Bronchoconstriction may be a normal means of restricting airflow and intake of irritants and allergens. Their long term use may actually increase exposure to these factors and cause more pronounced and chronic symptoms.
Anti-inflammatory agents have better long term effects.

Front 52

COPD

Back 52

Pathological changes that cause reduced expiratory air flow.
Does not change markedly over time.
Does not show major reversibility in response to pharmacological agents.
Progressive.
Assoc'd w/ abnormal inflammatory response of the lungs to noxious particles or gases.
Primary cause is smoking, both active and passive.
Other risks include occupational exposures and air pollution and genetic susceptibilities.

Front 53

Chronic bronchitis

Back 53

Hypersecretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years, usually in winter.

Front 54

Pathophysiology of chronic bronchitis

Back 54

Inspired irritants result in inflammation of the airways w/ infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall.
Causes bronchial edema and increases size and number of mucus glands and goblet cells.
Mucus is thick and tenacious, and can't be cleared b/c of impaired ciliary function.
Increases susceptibility to infection and injury.
Airways collapse in early expiration, blocked by mucus, and air is trapped in distal portion of the tract.
Leads to ventilation/perfusion mismatch.
Hypoxemia occurs.
Air trapping prevents respiratory muscles from functioning efficiently (barrel chest), and get hypoventilation and hypercapnia.

Front 55

Treatment of chronic bronchitis

Back 55

Best treatment is PREVENTION b/c changes are not reversible.
Cessation of smoking halts progression of the disease.
Bronchodilators, expectorants, and chest physical therapy are used prn.
Chronic oral steroids as a last resort.

Front 56

emphysema

Back 56

Abnormal, permanent enlargement of the gas-exchange airways and destruction of the alveolar walls.
Obstruction results from changes in lung tissue rather than mucus production and inflammation.
Major mechanism is loss of elastic recoil.
Major cause is smoking but also air pollution and childhood respiratory infections.
Primary emphysema linked to an inherited deficiency of the enzyme alpha-1 antitrypsin which inhibits the action of many proteolytic enzymes which can affect lung tissue.

Front 57

Pathophysiology of emphysema

Back 57

Begins w/ destruction of the alveolar septa, which eliminates potions of the capillary bed and increases the volume of air in the alveolus.
Inhaled oxidants inhibit the activity of endogenous antiproteases, and stimulate inflammation w/ increased activity of proteases.
See cont'd alveolar loss and loss of elastic recoil.
Expiration becomes difficult.
Hyperinflation of alveoli produce large air spaces called bullae and air spaces adjacent to the pleura called Blebs.
These aren't effective in gas exchange and result in hypoxemia.
Air trapping causes hyper expansion of the chest, which puts respiratory muscles at a mechanical disadvantage - can result in hypoventilation and hypercapnia late in the disease.

Front 58

Clinical manifestations of emphysema

Back 58

Dyspnea
Barrel chest
Minimal wheezing
Prolonged expiration
Hypoventilation and polycythemia late in the disease.

Front 59

Treatment of emphysema

Back 59

Similar to chronic bronchitis
Smoking cessation
Bronchodilating drugs
Antibiotics for acute infections.
Some can benefit from lung reduction surgery or lung transplant.

Front 60

Prerenal disease

Back 60

Results from inadequate blood flow to the kidney, which can be caused by decreased intravascular volume, lesions in the renal arteries, or hypotension.
Systemic disorders that decrease urine output.

Front 61

Renal disease

Back 61

Results from direct damage to the nephron.
Glomerular disorders.
Tubulointerstitial disorders which are disorders of the medullary tubules and interstitial cells.

Front 62

Postrenal disease

Back 62

Commonly due to urinary tract obstruction, which can be caused by kidney stones or tumors of the bladder, ureters, or prostate gland.

Front 63

Obstructive disorders

Back 63

Impedes flow proximal to blockage.
Dilates urinary system.
Increases risk for infection.
Compromises renal function.
Anatomic changes are called obstructive uropathy.

Front 64

Causes of obstruction

Back 64

Congenital malformations
Stones
Abdominal tumor or inflammation or scarring.
Tumor of urinary system or prostate.
Severe pelvic organ prolapse in women.

Front 65

What does renal obstruction cause dilation of?

Back 65

Dilation of ureters - hydroureter
Dilation of pelvis and calyces - hydronephrosis
Dilation of both - ureterohydronephrosis.

Front 66

What can result from renal dilation?

Back 66

Enlargement and fibrosis of distal nephron in 7 days.
Interference w/ distal and proximal nephron in 14 days.
Damage to glomeruli in 28 days.
Also see reduction in cortex and medulla.
Initial tubular damage decreases the ability to concentrate urine, causing an increase in urine volume.
The affected kidney can't conserve water, sodium, bicarbonate, or excrete potassium or hydrogen ions - leads to metabolic acidosis and dehydration.

Front 67

Complete renal obstruction can cause?

Back 67

Complete obstruction can lead to damage to tubules w/in hours, and irreversible w/in 4 weeks.

Front 68

Partial renal obstruction can cause?

Back 68

Partial obstruction can lead to permanent impairment of the ability to concentrate urine, resorb bicarbonate, excrete ammonia, or regulate acid-base balance.

Front 69

How does the body compensate for damage to one kidney?

Back 69

The body can partially compensate if one kidney is affected by compensatory hypertrophy of the other kidney.
NO increase in number of nephrons, but do see an increase in size of glomerulus and tubules.
This ability to compensate decreases w/ age.
Compensation is reversible if the other kidney recovers.

Front 70

Postobstructive diuresis

Back 70

Relief of partial obstruction of both kidneys or complete obstruction of one kidney results in post obstructive diuresis.
Usually mild and restores fluid and electrolyte balance.
Occasionally, can result in urine output of 10L/day.
Can cause dehydration and electrolyte imbalance.

Front 71

Obstruction of urethra

Back 71

Affects upper and lower tracts
Partial obstruction can lead to over active bladder and urine retention.
Can back up and cause hydroureter, hydronephrosis, and impaired kidney function.
Urine can be a microbiological growth medium - infection of obstructed kidney can cause further damage and scarring.

Front 72

How can obstruction of the urethra cause htn?

Back 72

The renin-angiotensin pathway in acute unilateral obstruction.
Due to water, sodium, and urea retention in chronic bilateral partial obstruction.

Front 73

Renal calculi

Back 73

Kidney stones
Masses of crystals, protein, or other substances.
Common cause of obstruction in adults.
Recurrence w/in 10 years is 50%.
Seen more in men.
Less risk if physically active and drink adequate water.
Calcium oxalate or phosphate is most common stone type.

Front 74

What can cause renal caliculi?

Back 74

Get increased concentrations of stone forming molecules in the urine w/ increased renal excretion of these molecules due to increased blood levels, decreased urine volume, and a change in urine pH.
Alkaline urine increases risk of calcium phosphate stones.
Acidic urine increases risk of uric acid stones.

Front 75

Clinical manifestations of renal caliculi

Back 75

Pain (renal colic) can determine location.
Nausea and vomiting
Chills and fever
Hematuria

Front 76

Treatment of renal caliculi

Back 76

UA and analysis of stones.
Removal by surgery - percutaneous lithotripsy.
Drugs to dissolve stones.

Front 77

Prevention of renal caliculi/future caliculi

Back 77

Treat underlying metabolic disorders.
Water intake = urine output of 2-3L/day.
Reduction in dietary oxalates and animal protein for uric acid stones.
Increased dietary fiber.
Do NOT decrease calcium intake - this increases risk of stones.

Front 78

Cystitis

Back 78

Inflammation of the bladder

Front 79

Symptoms of cystitis

Back 79

Urinary frequency
dysuria - painful or difficult urination.
Urgency
Lower abdominal, lower back or suprapubic pain.

Front 80

What is the cause of most UTI's?

Back 80

Gram negative bacteria of the intestinal tract
80% by E.coli - can form pili allowing bacterium to adhere to bladder epithelium
Cranberry and blueberry juice decreases bacterial adhesions by epicatechin.

Front 81

Treatment of UTI

Back 81

Antibiotics
Drink normal amounts of water, but avoid bladder irritants, such as caffeine.

Front 82

Nonbacterial cystitis

Back 82

Same symptoms but w/o infection.
Dysfunction of external sphincter, urethritis, or inflammation of glands near the vagina.

Front 83

Interstitial cystitis

Back 83

May be due to an autoimmune reaction, mucus deficiency, or abnormal mast cells.

Front 84

Two major functions of the kidneys

Back 84

Filtration of blood - removes metabolic wastes especially nitrogen containing waste.
Regulation of blood volume and composition, electrolytes, blood pH, and blood pressure.

Front 85

Nephron

Back 85

Functions in filtration, tubular reabsorption, and tubular secretion.
Consists of the renal corpuscle, proximal convoluted tubule, nephron loop of Loop of Henle, distal convoluted tubule, and collecting duct.

Front 86

Renal corpuscle

Back 86

In the nephron, the capillary containing glomerulus in the glomerular or Bowman's capsule.
Bowman's capsule receives filtrate.

Front 87

Proximal convoluted tubule

Back 87

Reabsorption of water and solutes.

Front 88

Nephron loop or Loop of Henle

Back 88

Regulate concentration of urine

Front 89

Distal convoluted tubule and collecting duct

Back 89

Reabsorption of water and electrolytes
Tubular secretion
Affected by ADH, aldosterone, and ANP.

Front 90

juxtaglomerular apparatus

Back 90

Juxtaglomerular cells lie in the wall of the afferent arteriole.
Macula densa in final portion of the Loop of Henle monitors sodium and chloride concentrations as well as water.
Controls blood flow into the glomerulus and also glomerular filtration.

Front 91

By the end of the proximal tubule, what has been absorbed?

Back 91

60-70% of water and sodium
About 100% of glucose and amino acids
90% of potassium, bicarbonate, calcium, and uric acid.

Front 92

Blood urea nitrogen (BUN)

Back 92

Urea is produced by the breakdown of amino acids.
If the GFR decreases due to renal disease, renal blockage, or decreased blood flow to the kidney, the BUN increases.

Front 93

Creatinine clearance

Back 93

Creatinine is an end product of muscle metabolism.
An indirect measure of GFR and renal blood flow.
Creatinine is neither reabsorbed or secreted, just freely filtered., so the amount excreted equals the amount filtered.

Front 94

Tubulointerstitial disorders

Back 94

Acute pyelonephritis
Urinary obstruction and reflux of urine are the most common risk factors.
Can involve one or both kidneys.
Most common in women.
Usually by ascending micro-organisms, but can be carried in blood.
May also be due to effects of drug and toxins.

Front 95

Acute pyelonephritis

Back 95

A tubulointerstitial disorder
Inflammation is usually focal and affects the renal pelvis, calyces, and medulla.
Glomeruli usually NOT involved.
Kidney is infiltrated w/ WBC's - pyuria.
Healing involves scarring and atrophy of affected tubules.

Front 96

Clinical manifestations of acute pyelonephritis

Back 96

Acute onset
Fever or chills
HA
Flank or groin pain
Dysuria and frequencey.
To distinguish from cystitis - LOOK FOR WHITE CELL CASTS.
Treatment w/ specific antibiotics.

Front 97

Chronic pyelonephritis

Back 97

More likely in patients w/ reflux or renal stones.
Scarring can lead to impaired urine-concentrating ability, leading to chronic renal failure.
May be due to drug toxicity from analgesics, such as aspirin, phenacetin, or acetaminophen.
Severe htn is often a contributing factor.

Front 98

Clinical manifestations of chronic pyelonephritis

Back 98

Often minimal and include htn, frequency and dysuria, and flank pain.
Diagnosis by UA or intravenous pyelography, ultrasound.
Treatment is to relieve obstruction and antibiotics.

Front 99

Glomerular disorders

Back 99

Due to a change or dysfunction of the glomerular capillaries
See changes in membrane permeablilty, GFR, protein or blood cells in urine.
Systemic changes include htn, edema, and acid-base and electrolyte imbalances.

Front 100

Glomerulonephritis

Back 100

Most commonly caused by an ABNORMAL IMMUNE RESPONSE.
Can be diffuse, focal, or segmental.
Can be membranous, proliferative, sclerotic, or crescentic.

Front 101

Acute glomerulonephritis

Back 101

OFTEN ASSOCIATED W/ STREPTOCOCCAL INFECTION.
Abrupt onset 7-12 days after strept throat or skin infection (impetigo).
Can also be caused by staphylococcus or viruses.
Strep antigens deposit in glomerular basement membrane and attract neutrophils and macrophages, initiating phagocytosis and release of inflammatory mediators that damage cells on BOTH sides of the basement membrane.

Front 102

Symptoms of acute glomerulonephritis

Back 102

Hematuria
Proteinuria
Dcreased GFR, oliguria or anuria
Htn
Edema around eyes, feet, and ankles.
Ascites or pleural effusion.

Front 103

Rapidly progressive GN

Back 103

Primarily adults in 50's and 60's.
May be idiopathic or associated w/ a proliferative disease.
Renal insufficiency by the time of diagnoses.
Proliferation of cells in Bowman's space w/ crescent formation.
Hematuria is common and may also see proteinuria, edema or htn.

Front 104

Goodpasture syndrome

Back 104

Antibody formation against pulmonary and glomerular capillary basement membranes.
Activation of complement and neutrophils damages glomerular basement membrane.
Primarily men 20-30 years old.
Can cause pulmonary hemorrhage and renal failure.

Front 105

Treatment of Goodpasture syndrome

Back 105

Treatment must begin early or prognosis is poor.
Anticoagulants reduce fibrin content of crescents.
Plasmapheresis w/ steroids and immunosuppression therapy

Front 106

Chronic glomerulonephritis

Back 106

Several diseases w/ a progressive course leading to chronic renal failure.
Two patters - deposition of antigen-antibody complexes, or antigens specific for GBM.
Complement activation and phagocyte activity damage capillary walls and cause proliferation of extracellular matrix, affecting GFR.

Front 107

Clinical manifestations of chronic GN

Back 107

Initially see increased membrane permeability and lose cells (hematuria) or protein into urine (proteinuria).
Fibrin is deposited into Bowman's space - crescent formation.
Renal blood flow and GFR is reduced.
Hematuria - smoky brown-tinged urine as opposed to pink or red.
Decreased GFR leads to fluid retention and htn.
Renal insufficiency progresses to renal failure after 10-20 years.

Front 108

Treatment of chronic GN

Back 108

Treat underlying disease
Steroids do NOT change the course of the disease.
Correct accompanying problems such as volume and b/p disorders.
Ultimately dialysis or transplant.

Front 109

Nephrotic syndrome

Back 109

Defined as excretion of 3.5 or more grams of protein per day.
Characteristic of glomerular injury.
Also see hypoalbuminemia, edema, hyperlipidemia
Loss of immunoglobulins can increase susceptibility to infections
DECREASE IN VITAMIN D.

Front 110

Treatment of Nephrotic syndrome

Back 110

Low-fat and salt restricted diet, but normal protein.
Diuretics
Immunosuppression
Protein supplements
Removal of glomerular membrane toxic factor.

Front 111

Nephritic syndrome

Back 111

Alteration of filtration leads to loss of RBC's.
Also see decreased GFR which causes decreased urine output, azotemia (increased nitrogenous wastes in the blood), and renal tubules undergo disuse atrophy and scarring.

Front 112

Most common cause of acute renal failure

Back 112

Prerenal is the most common cause.
Failure to restore blood volume or b/p and oxygen levels can lead to acute tubular necrosis or acute cortical necrosis.

Front 113

Intrarenal acute renal failure

Back 113

Usually due to acute tubular necrosis.
Usually caused by ischemia most often after surgery.
Whatever the case, get decreased GFR and oliguria.

Front 114

Postrenal acute renal failure

Back 114

Usually due to urinary tract obstruction that affects both kidneys.
Characterized by several hours of anuria w/ flank pain, followed by polyuria.

Front 115

Three stages of acute renal failure

Back 115

Stage 1 - Oliguria
Stage 2 - Diuresis
Stage 3 - Recovery

Front 116

Stage 1 of ARF

Back 116

Oliguria
Urine volume a/b 25% of normal to anuria.
Increased BUN and plasma creatinine.
Increased potassium (hyperkalemia) and electrolyte imbalance.
Fluid retention and edema
Congestive heart failure

Front 117

Stage 2 of ARF

Back 117

Diuresis
3-4 L/day of urine
Tubules still damaged, but recovering,
Can lose too much sodium and potassium and may see extracellular volume depletion

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Stage 3 of ARF

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Recovery
May take 3-12 months for plasma creatinine to return to normal.
A/b 30% never regain norma kidney function.

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Treatment of Acute renal failure

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Prevention if possible
Correct fluid and electrolyte imbalances
Treat infections
Maintain nutrition and cardiac function
DRUGS AND/OR MEDICATIONS ARE NOT EXCRETED.

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Chronic renal failure

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Progressive and irreversible loss of nephrons.
Alterations in salt and water balance not apparent until renal function is less than 25% of normal.
Common causes include chronic GN and chronic pyelonephritis.

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Clinical manifestations of chronic renal failure

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Often described w/ the term uremia - symptoms due to accumulation of toxins in plasma.
htn, anorexia, anemia, edema, pruritis (itching), CV disease, weight loss.

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Diagnoses of chronic renal failure

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Diagnosis is by increased BUN and serum creatinine.
Imaging will show small kidneys
Management includes restricting proteins and potassium in the diet, evaluating fluid and sodium levels.
Treatment w/ erythropoietin as needed.